Protective Role of miR‐432‐5p Against Propofol‐Induced Neurotoxicity Through Regulation of ITK in SH‐SY5Y Cells

The widespread use of propofol in pediatric anesthesia raises significant concerns regarding its potential neurodevelopmental toxicity and long-term cognitive impairment in children. To explore the protective role of miR-432-5p against propofol-induced neurotoxicity and clarify its underlying mechanisms mediated by targeting interleukin-2-inducible T-cell kinase (ITK). An in vitro model of propofol-induced damage was constructed using the SH-SY5Y cell line. Cell survival, the percentage of apoptosis, and the secretion of pro-inflammatory factors (TNF-α, IL-1β, and IL-6) were subsequently quantified. Finally, the direct interaction between miR-432-5p and its target, ITK, was verified through dual-luciferase reporter assays. miR-432-5p was markedly downregulated following propofol exposure. In vitro, miR-432-5p overexpression improved cell viability, reduced apoptosis, and suppressed pro-inflammatory cytokine release. ITK was validated as a direct downstream target of miR-432-5p. Furthermore, compensatory overexpression of ITK partially reversed the anti-apoptotic and anti-inflammatory protective phenotypes induced by miR-432-5p. The miR-432-5p/ITK regulatory axis significantly mitigates propofol-induced cellular injury by restraining apoptosis and neuroinflammation. Maintaining miR-432-5p abundance provides a promising theoretical basis and therapeutic target for preventing anesthesia-related cognitive impairment.